Lingling Li

Shanghai Changzheng Hospital

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Xiaolan Zhao

Memorial Sloan Kettering Cancer Center

Yujue Wang

Shenzhen Institutes of Advanced Technology

Xun Zhang

Hubei University

Xiaojiao Wang

Obstetrics and Gynecology Hospital of Fudan University

Chunyi Gu

Obstetrics and Gynecology Hospital of Fudan University

Zhao Wu

Guangzhou Medical University

Xiaohong Deng

Beijing Obstetrics and Gynecology Hospital

Zhenrong Zheng

University of Electronic Science and Technology of China

Jie Mei

Nanjing Drum Tower Hospital

Fangyuan Luo

West China Second University Hospital of Sichuan University

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University of Electronic Science and Technology of China

Fudan University

Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital

Obstetrics and Gynecology Hospital of Fudan University

First Affiliated Hospital of Zhengzhou University

Nanjing Medical University

Sichuan University

Shenzhen Bay Laboratory

Central South University

Shanghai Jiao Tong University

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Long non-coding RNA OIP5-AS1 suppresses microRNA-92a to augment proliferation and metastasis of ovarian cancer cells through upregulating ITGA6

Journal of Ovarian Research (2022)

Yujue Wang Lingling Li Xun Zhang Xiaolan Zhao

Recently, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as essential biomarkers during development of malignancies. This study was performed to study the roles of lncRNA opa-interacting protein 5 antisense transcript 1 (OIP5-AS1) and miR-92a in ovarian cancer (OC).OIP5-AS1, miR-92a and integrin alpha 6 (ITGA6) expression in OC tissues and cells was assessed. The screened OC cells were respectively with OIP5-AS1-, miR-92a- and ITGA6-related vectors or oligonucleotides . The viability, migration, invasion and apoptosis of the cells were determined and the levels of epithelial-mesenchymal transition (EMT)-related proteins were also measured. The interactions between OIP5-AS1 and miR-92a, and between miR-92a and ITGA6 were confirmed.OIP5-AS1 and ITGA6 were upregulated while miR-92a was downregulated in OC. Inhibited OIP5-AS1 or downregulated ITGA6 or elevated miR-92a repressed EMT, viability, migration and invasion, and promoted apoptosis of OC cells. OIP5-AS1 as a competing endogenous RNA interacted with miR-92a to regulate ITGA6. These effects that induced by silenced OIP5-AS1 could be reversed by miR-92a inhibition while those that induced by up-regulated miR-92a were reduced by restored ITGA6.OIP5-AS1 silencing promoted miR-92a to repress proliferation and metastasis of OC cells through inhibiting ITGA6.

Competing Endogenous RNA

10.1186/s13048-021-00937-3

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Spinal IL‐36γ/IL‐36R participates in the maintenance of chronic inflammatory pain through astroglial JNK pathway

Glia (2018)

Qian Li Shenbin Liu Lingling Li Xiaoli Ji Min Wang

Abstract Emerging evidence indicates that spinal neuroinflammation contributes to the maintenance of chronic inflammatory pain. IL‐36, as a novel member of the interleukin (IL)‐1 super‐family cytokines, plays an important role in inflammatory responses. The present study aimed to investigate the role of spinal IL‐36 and IL‐36 receptor (IL‐36R) signaling in the pathology of chronic inflammatory pain. IL‐36γ and IL‐36R, but not IL‐36α and IL‐36β, were persistently upregulated in the spinal cord of mice with intraplantar injections of complete Freund's adjuvant (CFA). Intrathecal administration of both IL‐36R antagonist (IL‐36Ra) and IL‐36γ siRNA significantly attenuated CFA‐induced chronic inflammatory pain behaviors. Furthermore, CFA‐induced IL‐36γ expression was mainly observed in spinal neurons whereas IL‐36R was primarily expressed in spinal astrocytes. Additionally, the intrathecal injection of IL‐36γ was sufficient to induce pain hypersensitivity and astrocyte activation in naive mice, and these effects could be inhibited by blocking c‐Jun N‐terminal kinase (JNK) phosphorylation. In vitro experiments also demonstrated that the IL‐36γ could induce astrocytic JNK activation and inflammatory cytokines release, which was mediated by IL‐36R. Finally, intrathecal injection of IL‐36γ‐activated astrocytes in a pJNK‐dependent manner induced mechanical allodynia and thermal hyperalgesia in naive mice. Collectively, these findings reveal that the neuronal/astrocytic interaction in the spinal cord by which neuronally produced IL‐36γ activates astrocytes via IL‐36R‐mediated JNK pathway is crucial for the maintenance of chronic inflammatory pain. Thus, IL‐36γ/IL‐36R‐mediated astrocyte signaling may be a suitable therapeutic target for chronic inflammatory pain.

Proinflammatory cytokine

Neuroglia

10.1002/glia.23552

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In situ formed scaffold with royal jelly-derived extracellular vesicles for wound healing

Theranostics (2023)

Dehong Tan Wenxiang Zhu Lujie Liu Yuanwei Pan Yangtao Xu

Safe and effective wound healing can be a major clinical challenge. Inflammation and vascular impairment are two main causes of inadequate wound healing.

Skin repair

10.7150/thno.84665

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Citations (25)